Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cardiobacterium

ABSTRACT: Endocarditis due to Cardiobacterium hominis

PROVIDER: PRJEB25228 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	ERR2356930_1.fastq.gz	Fastqsanger.gz
	ERR2356930_2.fastq.gz	Fastqsanger.gz
	ERR2356931_1.fastq.gz	Fastqsanger.gz
	ERR2356931_2.fastq.gz	Fastqsanger.gz
	ERR2356932_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

Cardiobacterium hominis

Project description:Cardiobacterium hominis overview

| PRJNA37685 | ENA

Draft genome sequence of Cardiobacterium hominis

Project description:Draft genome sequence of a Cardiobacterium hominis strain isolated from blood cultures of a patient with infective endocarditis

| PRJEB13157 | ENA

Cardiobacterium valvarum

Project description:Cardiobacterium valvarum overview

| PRJNA50003 | ENA

Cardiobacterium valvarum

Project description:Whole genome sequencing of Cardiobacterium valvarum, an opportunistic pathogen

| PRJDB2862 | ENA

Microbiome patterns analysis of Tuberculosis, Non-Tuberculous Mycobacteria and other respiratory patients

Project description:Tuberculosis (TB) and non-tuberculous mycobacterial (NTM) infections, though clinically similar, require distinct management, highlighting the need for reliable biomarkers to differentiate them. In a study of 108 patients, 16S rRNA sequencing revealed distinct microbial signatures, with Enterococcus faecalis, Streptococcus mutans, and Snodgrassella alvi associated with TB, and Cardiobacterium hominis and Prevotella nigrescens linked to NTM. The absence of Mobiluncus curtisii, particularly with Olsenella phocaeensis also absent, suggested a higher probability of NTM, offering promising insights for diagnostic and therapeutic advancements.

2025-12-02 | GSE278953 | GEO

Neisseria

Project description:Endocarditis due to Neisseria meningitidis

| PRJEB24753 | ENA

Transcription profiling of human monocytes and monocyte-derived macrophages infected with Coxiella burnetii and incubated with apoptotic or necrotic lymphocytes

Project description:Q fever is due to Coxiella burnetii, an obligate intracellular bacterium. We investigated the mechanism of establishment of chronic form of the Q fever that mainlym anifested by endocarditis. We showed that patients with acute Q fever and valvulopathy, who have the higher risk to develop an endocarditis, exhibited high levels of circulating apoptotic cells. We further investigated the effect of the uptake of dead cells on the intracellular fate of the bacterium and the immune response of monocytes and macrophages.

2008-10-09 | E-MEXP-1289 | biostudies-arrayexpress

Cell wall-deficient Mycoplasma hominis represses biofilm formation of uropathogenic Escherichia coli.

Project description:The features of Mycoplasma in human organ such lung and urinary tract are enigmatic. Here, the role of M. hominis in regard to biofilm formation of uropathogenic Escherichia coli (UPEC) strain CFT073 was investigated. Although M. hominis were inferred to not impact on UPEC bacterial fitness including growth and productions of signaling molecules as autoinducer-2 (AI-2) and indole, we found that the presence of M. hominis dramatically decreased biofilm formation of UPEC CFT073 as well as slightly repressed attachment and cytotoxicity of that. Importantly, this activity was observed on UPEC strain specifically, not enterohemorrhagic E. coli (EHEC) strain that exists on intestine. Whole-transcriptome profiling and quantitative real-time polymerase chain reaction (qRT-PCR) analysis revealed PhoPQ system and anti-termination protein (encoded by ybcQ) participates on the reduction of biofilm formation by M. hominis (corroborated by qRT-PCR). Furthermore, collaborating with previous report that toxin-antitoxin (TA) system involved in biofilm formation, M. hominis increased on the transcriptions of toxin genes including hha (toxin gene in Hha-TomB TA system) and pasT (toxin part in PasT-PasI TA system). Hence, we propose that one possible role of M. hominis is to influence bacterial biofilm formation in urinary tract. Only fourteen genes were induced (2.5-fold) by the presence of M. hominis in Uropathogenic Escherichia coli (UPEC) biofilm cells. Among upregulated genes, ybcQ (encodes anti-termination protein Q homolog) and phoP/phoQ (encode DNA-binding response regulators in two-component regulatory system), were induced by the presence of M. hominis. Two-condition experiment, UPEC CFT073 alone vs. UPEC CFT073 with Mycoplasma hominis PG21 (10^5 ccu/ml). For preparing the total RNA, UPEC CFT073 cells were grown at 37Â°C in biofilm cells on glass wool with or without M. hominis for 24 h.

2016-01-08 | E-GEOD-43376 | biostudies-arrayexpress

Endocarditis caused by Cardiobacterium valvarum.

Project description:A fastidious, gram-negative bacterium was isolated from the blood of a 51-year-old man who had acute infectious endocarditis (IE). Characterization of the organism through phenotypic and genotypic analyses revealed the causative role of Cardiobacterium valvarum. This is the third reported case of IE caused by C. valvarum.

| S-EPMC1392641 | biostudies-literature

Staphylococcus aureus delays wound repair by harnessing the agr quorum sensing system to target keratinocyte lipid metabolism [bulkRNA-seq]

Project description:NHEKs wounded by scratch and incubated with CM for 24 hours were evaluated by bulk RNAseq. Principal component analysis of these data revealed wounded NHEKs exposed to S. hominis products clustered close to control keratinocytes, suggesting these groups have similar transcriptomes, while the presence of S. aureus products caused variation shift in the transcriptome to result in a distinct cluster away from control. This was supported by a heatmap of differential gene expression of S. aureus and S. hominis CM treatment showing broad S. aureus-mediated suppression of genes induced by S. hominis. Conversely, upregulation of many genes by S. aureus were downregulated by S. hominis.

2025-08-02 | GSE273933 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data